Casado A, Casado C, López-Fernández E, de la Torre R
Departmento de Fisiopatología y Genetica Molecular Humana, Centro de Investigaciones Biologicas (CSIC), Madrid, Spain.
Panminerva Med. 1995 Dec;37(4):175-7.
Numerous findings have shown that enzyme deficiencies, especially those involved in the protection of red cells from oxidation may lead to hemolysis and hyperbilirubinemia. It is established that G6PD deficiency may be the cause of neonatal hyperbilirubinemia, as has been found in several countries and among widely different ethnic groups. We try to establish the incidence of G6PD, PK and GSSG-R deficiencies in neonates with jaundice for a better assessment of the population at risk. The present investigation was carried out in the attempt to be certain whether these enzymes could play a part in the development of neonatal jaundice. A total of 341 neonates of both sexes with jaundice were analyzed: 47 with G6PD deficiency; 9 with PK deficiency and 2 with GSSG-R deficiency.
众多研究结果表明,酶缺乏,尤其是那些参与保护红细胞免受氧化的酶缺乏,可能导致溶血和高胆红素血症。已证实,葡萄糖-6-磷酸脱氢酶(G6PD)缺乏可能是新生儿高胆红素血症的病因,在多个国家和广泛不同的种族群体中均有发现。我们试图确定黄疸新生儿中G6PD、丙酮酸激酶(PK)和谷胱甘肽还原酶(GSSG-R)缺乏的发生率,以便更好地评估高危人群。本次调查旨在确定这些酶是否在新生儿黄疸的发生中起作用。共分析了341例患黄疸的新生儿:47例有G6PD缺乏;9例有PK缺乏;2例有GSSG-R缺乏。